The role of glycoprotein H of equine herpesviruses 1 and 4 (EHV-1 and EHV-4) in cellular host range and integrin binding

Walid Azab; Lara Zajic; Nikolaus Osterrieder

doi:10.1186/1297-9716-43-61

The role of glycoprotein H of equine herpesviruses 1 and 4 (EHV-1 and EHV-4) in cellular host range and integrin binding

Research output: Journal Publications and Reviews (RGC: 21, 22, 62) › 21_Publication in refereed journal › peer-review

Overview

8 Scopus Citations

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Author(s)

Walid Azab
Lara Zajic
Nikolaus Osterrieder

Detail(s)

Original language	English
Article number	61
Journal / Publication	Veterinary Research
Volume	43
Online published	21 Aug 2012
Publication status	Published - 2012
Externally published	Yes

Link(s)

DOI	DOI https://doi.org/10.1186/1297-9716-43-61 Final Published version
	Check@CityULib
Attachment(s)	Documents 54719129.pdf Final Published version, 2.37 MB, PDF Publisher's Copyright Statement This full text is made available under CC-BY 2.0. https://creativecommons.org/licenses/by/2.0/
Link to Scopus	https://www.scopus.com/record/display.uri?eid=2-s2.0-84871209413&origin=recordpage
Permanent Link	https://scholars.cityu.edu.hk/en/publications/publication(2fe3a81e-bdb6-44cb-bdb2-3d45de013632).html

Abstract

Equine herpesvirus type 1 and 4 (EHV-1 and EHV-4) glycoprotein H (gH) has been hypothesized to play a role in direct fusion of the virus envelope with cellular membranes. To investigate gH's role in infection, an EHV-1 mutant lacking gH was created and the gH genes were exchanged between EHV-1 and EHV-4 to determine if gH affects cellular entry and/or host range. In addition, a serine-aspartic acid-isoleucine (SDI) integrin-binding motif present in EHV-1 gH was mutated as it was presumed important in cell entry mediated by binding to α4β1 or α4β7 integrins. We here document that gH is essential for EHV-1 replication, plays a role in cell-to-cell spread and significantly affects plaque size and growth kinetics. Moreover, we could show that α4β1 and α4β7 integrins are not essential for viral entry of EHV-1 and EHV-4, and that viral entry is not affected in equine cells when the integrins are inaccessible. © 2012 Azab et al.; licensee BioMed Central Ltd.